International audience | In recent decades, stormwater management has developed to allow stormwater to infiltrate directly into the soils instead of being collected and routed to sewer systems. However, during infiltration, stormwater creates a sediment deposit at the soil surface as the result of high loads of suspended particles (including pollutants), leading to the settlement of sedimentary layers prone to colonization by plants and earthworms. This study aims to investigate the earthworm communities of a peculiar infiltration basin and investigate the influence of edaphic conditions (water content, organic matter content, pH, height of sediment) and of persistent organic pollutants (POPs: PCBs, PCDDs and PCDFs) on these earthworms. Attention was paid to their age (juveniles or adults) and their functional group (epigeic, endogeic, anecic). We found that the earthworm abundance was mostly driven by edaphic conditions, with only a slight impact of POPs, with a significant negative impact of PCBDLno for juveniles and endogeic, and PCDDs for epigeic. On the contrary, the height of the sediment and the water content are beneficial for their presence and reproduction. Furthermore, POPs contents are also linked to physicochemical parameters of the sediment. Bioaccumulation was clearly revealed in the studied site but does not differ between juveniles and adults, except for PCDDs. Conversely, BAF values seemed to vary between functional groups, except for PCBDL non-ortho. It strongly varies with the family types (PCBs versus PCCD/Fs) and between congeners within the same family, with specific strong bioaccumulation for a few congeners.

Morphological tools can assist in the evaluation of effects of insecticides on non-target insects. Pyriproxyfen, a juvenile hormone analog, is known to interfere with growth and metamorphosis of insects. However, there are studies showing indirect effects on natural enemies, including green lacewings. Few prior studies describe morphological effects of pyriproxyfen on target insect organs, especially on natural enemies. Through morphological tools, this study aimed to characterize the midgut and fat body, both important organs of digestion and great metabolic activity respectively, of the predator Ceraeochrysa claveri after chronic exposure to pyriproxyfen. Larvae of C. claveri were fed Diatraea saccharalis egg clusters treated with pyriproxyfen in solution of 50 or 100 mg a.i. L⁻¹ throughout the larval stage. The biological data revealed significant increases in development time, especially in the third instar, and in cumulative mortality from the prepupal into the pupal stage. Morphological analysis of adult midgut (≤24 h old) showed damage including formation of epithelial folds, intercellular spaces, emission of cytoplasmic protrusions. Both fat body regions presented decrease of lipid droplets, vacuolization of trophocytes and mitochondrial injury featuring a multisystemic action. In both organs, pyriproxyfen exposure induced significant oxidative stress by mitochondrial superoxide production. Cytoprotective responses were induced in midgut and fat body cells by augmenting the number of cytoplasmic granules containing calcium and expression of HSP 90. Both organs proved to be efficient in presenting histopathological alterations, showing the sensitivity and applicability of this morphological tool for evaluating other insecticides in non-target organisms.

Lead concentrations in hard antlers of adult European roebucks (Capreolus capreolus) were analyzed to assess lead exposure of roe deer roaming the floodplain of the Innerste River, a river system contaminated due to historical metal ore mining, processing, and smelting in its upper reaches. Antler lead concentrations of roebucks culled in the period 1939–2018 within or close to the Innerste floodplain ranged between <0.17 mg Pb/kg (limit of detection) and 51.5 mg Pb/kg (air-dry weight). Median lead concentration in antlers of roebucks culled within the floodplain was 11.1 mg Pb/kg, compared to 2.3 mg Pb/kg in antlers of bucks culled in the floodplain vicinity (P < 0.01). Sampling year had no significant effect on antler lead concentrations (P = 0.748). Lead isotope ratios of antlers from the Innerste downstream area (²⁰⁶Pb/²⁰⁷Pb: 1.179–1.181; ²⁰⁸Pb/²⁰⁶Pb: 2.083–2.085) fell within the range of those reported for hydrothermal vein deposits from the upper catchment area of the Innerste River in the Harz Mountains. Our study demonstrates the long-lasting impact of the historical metal ore mining, processing, and smelting in the Harz Mountains on lead pollution in floodplains of rivers draining this area and the lead exposure of wild herbivores inhabiting the floodplains. Furthermore, it highlights the suitability of roe deer antlers for monitoring environmental lead levels and the usefulness of lead isotope signatures in antlers for source apportionment of lead pollution.

Exposure to endocrine disruptors such as bisphenols, can lead to and be the explanation for idiopathic infertility. In our study, we assessed the effect of exposure to bisphenol S (BPS) via breast milk on the testicular tissue health of adult male mice. Milking dams were exposed to BPS through drinking water (0.216 ng g bw/day and 21.6 ng g bw/day) from post-natal day 0–15. Although there was no significant difference in testicular histopathology between the control and experimental groups, we observed an increase in the number of tight and gap junctions in the blood-testis barrier (BTB) of adult mice after nursing BPS exposure. Moreover, there was an increase in oxidative stress markers in adult testicular tissue of mice exposed during nursing. Our nursing model indicates that breast milk is a route of exposure to an endocrine disruptor that can be responsible for idiopathic male infertility through the damage of the BTB and weakening of oxidative stress resistance in adulthood.

Endocrine-disrupting chemicals (EDCs) are ubiquitous in daily life, but their harmful effects on the human body have not been fully explored. Recent studies have shown that EDCs exposure could lead to infertility, menstrual disorder and menopause, resulting in subsequent effects on female health. Therefore, it is of great significance to clarify and summarize the impacts of EDCs on ovarian aging for explaining the etiology of ovarian aging and maintaining female reproductive health. Here in this review, we focused on the impacts of ten typical environmental contaminants on the progression of ovarian aging during adult exposure, including epidemiological data in humans and experimental models in rodents, with their clinical phenotypes and underlying mechanisms. We found that both persistent (polychlorinated biphenyls, perfluoroalkyl and polyfluoroalkyl substances) and non-persistent (phthalates) EDCs exposure could increase an overall risk of ovarian aging, leading to the diminish of ovarian reserve, decline of fertility or fecundity, irregularity of the menstrual cycle and an earlier age at menopause, and/or premature ovarian insufficiency/failure in epidemiological studies. Among these, the loss of follicles can also be validated in experimental studies of some EDCs, such as BPA, phthalates, parabens and PCBs. The underlying mechanisms may involve the impaired ovarian follicular development by altering receptor-mediated pro-apoptotic pathways, inducing signal transduction and cell cycle arrest and epigenetic modification. However, there were inconsistent results in the impacts on fertility/fecundity, menstrual/estrous cycle and hormone changes response to different EDCs, and differences between human and animal studies. Our review summarizes the current state of knowledge on ovarian disrupters, highlights their risks to ovarian aging and identifies knowledge gaps in humans and animals. We therefore propose that females adopt healthy lifestyle changes to minimize their exposure to both persistent and non-persistent chemicals, that have the potential damage to their reproductive function.

Multigenerational tests provide a comprehensive assessment of the long-term toxicity of pollutants. Here, the multigenerational effects of soil metal contamination on Folsomia candida were investigated over five generations (generations 1–5: F1–F5). Nine soils with varying physicochemical properties and degrees of metal pollution were studied. The selected endpoints were survival, reproduction, body size and body metal concentrations. F. candida was cultured only up to the fifth generation with high reproduction in contaminated acid soils where reproduction was at least 5 times that in neutral soils and 20 times that in calcareous soils. Correlation analysis indicated that soil pH (68.9% contribution) and cation exchange capacity (CEC, 15.4% contribution) were more important factors than pollution level affecting the reproduction of F. candida. No significant difference was observed in adult survival or adult length over five generations. The highest collembolan body Cd concentrations in soils A1-A3 were 3.15, 2.93 and 3.23 times those in F1, with similar results for body Pb. A similar trend in reproduction and juvenile length was observed with an initial decrease (p < 0.05) and then an increase (p < 0.05) over the generations in each acid soil; the opposite trend occurred in the changes in body cadmium (Cd) and lead (Pb) concentrations which increased initially (p < 0.05) and then decreased (p < 0.05) compared to the original concentrations of the first generation. The results indicate that F. candida can adapt to soil metal stress during multigenerational exposure and the adaption energy may be related to a tradeoff between reproduction or growth of juveniles and the detoxification of metals accumulated in the body. Soil properties, especially pH and CEC, had a substantial influence on the long-term survival of the collembolan in the metal-polluted soils.

Perfluorooctanesulfonic acid (PFOS) is a persistent anthropogenic chemical that can affect the thyroid hormone system in humans and animals. In adults, thyroid hormones (THs) are regulated by the hypothalamic-pituitary-thyroid (HPT) axis, but also by organs such as the liver and potentially the gut microbiota. PFOS and other xenobiotics can therefore disrupt the TH system at various locations and through different mechanisms. To start addressing this, we exposed adult male rats to 3 mg PFOS/kg/day for 7 days and analysed effects on multiple organs and pathways simultaneously by transcriptomics. This included four primary organs involved in TH regulation, namely hypothalamus, pituitary, thyroid, and liver. To investigate a potential role of the gut microbiota in thyroid hormone regulation, two additional groups of animals were dosed with the antibiotic vancomycin (8 mg/kg/day), either with or without PFOS. PFOS exposure decreased thyroxine (T4) and triiodothyronine (T3) without affecting thyroid stimulating hormone (TSH), resembling a state of hypothyroxinemia. PFOS exposure resulted in 50 differentially expressed genes (DEGs) in the hypothalamus, 68 DEGs in the pituitary, 71 DEGs in the thyroid, and 181 DEGs in the liver. A concomitant compromised gut microbiota did not significantly change effects of PFOS exposure. Organ-specific DEGs did not align with TH regulating genes; however, genes associated with vesicle transport and neuronal signaling were affected in the hypothalamus, and phase I and phase II metabolism in the liver. This suggests that a decrease in systemic TH levels may activate the expression of factors altering trafficking, metabolism and excretion of TH. At the transcriptional level, little evidence suggests that the pituitary or thyroid gland is involved in PFOS-induced TH system disruption.

Organochlorine contaminants (OCs) – organochlorine pesticides (OCPs) and industrial products and byproducts – are included in different monitoring programmes and surveys, involving various animal species. Fish-eating birds are suitable indicator species for OCs. Adult birds may be difficult to capture, but chicks can be sampled more easily. Blood of birds is a potentially suitable non-destructive matrix for analysis, as OC levels in blood reflect their concentrations in the body. The study was aimed at investigating how age of fast-growing Grey heron (Ardea cinerea) chicks affects contaminant levels in their blood and thus how important is sampling at exact age for biomonitoring purposes. In 1999 on Lake Engure in Latvia whole blood samples of heron chicks were collected at three different time points, with seven and nine days in between the first and second and second and third sampling points, respectively. Twenty-two chicks were sampled at all three times. In total, 102 samples were analysed for 19 polychlorinated biphenyl (PCB) congeners, DDT metabolites – DDE and DDD, hexachlorobenzene (HCB), α-, β-, γ-hexachlorocyclohexane (HCH), and trans-nonachlor. Total PCB concentrations averaged around 2000 ng/g dry extracted matter (EM). DDE was the dominant individual contaminant (ca. 800 ng/g EM), followed by CB-153, -138, and −118. Most of the other analysed OCs were below 100 ng/g EM. No significant (p > 0.05) differences in OC concentrations were found between the three sampling occasions, except for trans-nonachlor. This means that blood can safely be sampled for biomonitoring purposes during the 17 days’ time window. The analysed legacy contaminants may serve as model substances for other persistent organic pollutants.

This study focused on the impacts of aged aquaculture microplastics (MPs) on oysters (Crassostrea gigas). Adult oysters were exposed for two months to a cocktail of MPs representative of the contamination of the Pertuis Charentais area (Bay of Biscay, France) and issuing from oyster framing material. The MPs mixture included 28% of polyethylene, 40% of polypropylene and 32% of PVC (polyvinyl chloride). During the exposure, tissues were sampled for various analyzes (MP quantification, toxicity biomarkers). Although no effect on the growth of adult oysters was noted, the mortality rate of bivalves exposed to MPs (0.1 and 10 mg. L⁻¹ MP) increased significantly (respectively 13.3 and 23.3% of mortalities cumulative). On the one hand, the responses of biomarkers revealed impacts on oxidative stress, lipid peroxidation and environmental stress. At 56 days of exposure, significant increases were noted for Glutathione S-Transferase (GST, 10 mg. L⁻¹ MP), Malondialdehyde (MDA, 10 mg. L⁻¹ MP) and Laccase (LAC, 0.1 and 10 mg. L⁻¹ MP). No variations were observed for Superoxyde Dismutase (SOD). Besides, ingestion of MPs in oyster tissues and the presence in biodeposits was highlighted. In addition, in vitro fertilisations were performed to characterize MPs effects on the offspring. Swimming behavior, development and growth of D-larvae were analysed at 24-, 48- and 72-h after fertilisation. D-larvae, from exposed parents, demonstrated reduced locomotor activity. Developmental abnormalities and arrest as well as growth retardation were also noted. This study highlighted direct and intergenerational effects of MPs from aged plastic materials on Pacific oysters.

Long-term exposure to PM₂.₅ has been linked to lung cancer incidence and mortality, but limited evidence existed for other cancers. This study aimed to assess the association between PM₂.₅ on cancer specific mortality. An ecological study based on the cancer mortality data collected from 5,565 Brazilian cities during 2010–2018 using a difference-in-differences approach with quasi-Poisson regression, was applied to examine PM₂.₅-cancer mortality associations. Globally gridded annual average surface PM₂.₅ concentration was extracted and linked with the residential municipality of participants in this study. Sex, age stratified and exposure-response estimations were also conducted. Totalling 1,768,668 adult cancer deaths records of about 208 million population living across 5,565 municipalities were included in this study. The average PM₂.₅ concentration was 7.63 μg/m³ (standard deviation 3.32) with range from 2.95 μg/m³ to 28.5 μg/m³. With each 10 μg/m³ increase in three-year-average (current year and previous two years) concentrations of PM₂.₅, the relative risks (RR) of cancer mortality were 1.16 (95% confidence interval [CI]: 1.11–1.20) for all-site cancers. The PM₂.₅ exposure was significantly associated with several cancer-specific mortalities including oral, nasopharynx, oesophagus, and stomach, colon rectum, liver, gallbladder, larynx, lung, bone, skin, female breast, cervix, prostate, brain and leukaemia. No safe level of PM₂.₅ exposure was observed in the exposure-response curve for all types of cancer. In conclusion, with nationwide cancer death records in Brazil, we found that long-term exposure to ambient PM₂.₅ increased risks of mortality for many cancer types. Even low level PM₂.₅ concentrations had significant impacts on cancer mortality.